Background: Three genes encode human nonmuscle myosin II (NM II) heavy chains, and the proteins have different intracellular roles and localizations. Results: NM II paralogs form bipolar filaments, but there are important differences in filament structure, enzymatic, and actin binding behavior. Conclusion: NM II filaments show diverse interactions with actin. Significance: NM II filaments are adapted to work in cytoskeletal networks.

No abstract

Mesenchymal stem cells (MSCs) have been demonstrated to be involved in tumor progression and the modulation of the tumor microenvironment, partly through their secretome. Extracellular vesicles (EVs) are membranous nanovesicles secreted by multiple types of cells and have been demonstrated to mediate intercellular communication in both physiological and pathological conditions. However, numerous questions still remain regarding the underlying mechanisms and functional consequences of these interactions. The purpose of this study was to investigate the effects of human umbilical cord mesenchymal stem cell-derived EVs (hUC-MSC-EVs) on the proliferation, migration and invasion of human breast cancer cells. We successfully generated and identified hUC-MSCs and hUC-MSC-EVs which were used in this study. The results revealed that treatment of the MDA-MB-231 and MCF-7 human breast cancer cells with medium containing hUC-MSC-EVs significantly enhanced the proliferation, migration and invasion of the cells in vitro. Treatment of the cells with medium containing hUC-MSC-EVs also reduced E-cadherin expression and increased N-cadherin expression, thus promoting the epithelial-mesenchymal transition (EMT) of the breast cancer cells. Treatment of the breast cancer cells with extracellular signal-regulated kinase (ERK) inhibitor prior to the interaction with hUC-MSC-EVs significantly reversed the enhanced proliferation, migration and invasion, as well as the EMT of the breast cancer cells induced by the hUC-MSC-EVs. On the whole, these data indicate that hUC-MSC-EVs promote the invasive and migratory potential of breast cancer cells through the induction of EMT via the ERK pathway, leading to malignant tumor progression and metastasis. Taken together, the findings of this study suggest that targeting pathways to reverse EMT may lead to the development of novel therapeutic approaches with which to combat breast cancer.

Abstract. microRNAs are involved in different cancer-related processes. miR-195, one of the miR-16/15/195/424/497 family members, has been shown to act as a tumor suppressor during tumorigenesis. However, the function of miR-195 in osteosarcoma is still unclear. In our study, the miR-195 expression level was upregulated in osteosarcoma cells, by transfection with miR-195, and the fatty acid synthase (FASN) mRNA and protein expression levels were measured by RT-PCR and western blotting. Cell migration and invasion was measured using wound healing migration and Transwell invasion assays. We found that the upregulation of miR-195 greatly decreased cell invasion and the migration of U2OS. We also identified that FASN may be a direct target of miR-195 by the luciferase activity assay. These findings provide evidence that miR-195 plays a key role in inhibiting osteosarcoma cell migration and invasion through targeting FASN, and strongly suggest that exogenous miR-195 may have therapeutic value in treating osteosarcoma.